Investigation of PEG directed Sb2WO6 for dyes removal from wastewater.

Pristine and polyethylene glycol assisted antimony tungstate (Sb2WO6) was developed via hydrothermal route. The pristine and surfactant assisted Sb2WO6 were further exemplified to reveal the properties of the samples. The bandgap calculated for Sb2WO6, 5 ml PEG- Sb2WO6, 10 ml PEG- Sb2WO6 was 2.78 eV, 2.66 eV and 2.21 eV. The 10 ml PEG assisted sample exhibited narrow bandgap. The Fourier transform infrared spectroscopy (FTIR) spectra of the samples showed metal vibrations and stretching of the water molecules adsorbed. The Raman spectra showed the vibrational modes present in Sb2WO6. The morphology was analyzed employing transmission electron microscope (TEM) for all samples. Pristine Sb2WO6 showed growth of nanorods with higher dimensions with high agglomeration. 5 ml PEG- Sb2WO6 showed the growth of nanorods with lesser agglomeration. 10 ml PEG assisted Sb2WO6 exhibited distinct growth of nanorods with no agglomeration on the surface. The elemental composition was examined employing X-ray Photoelectron Spectroscopy. Prepared product photocatalytic behaviour was tested employing Rhodamine B dye degrading. Different catalyst loading were investigated for degrading the toxic pollutants. 0.2 g 10 ml PEG-Sb2WO6 showed 81% efficiency on degrading the toxic pollutant from wastewater. The OH radicals are accountable for photocatalytic behaviour of prepared photocatalyst. The 10 ml PEG-Sb2WO6 has the good reusability behavior and stable properties after three cycles. The prepared 10 ml PEG- Sb2WO6 photocatalyst will be the potential candidate for the remediation of the water treatment.

A novel flexible drill device enabling arthroscopic transosseous repair of Bankart lesions.

We have developed a flexible drill device that makes arthroscopic transosseous repair possible, and report preliminary results. Twelve patients with post-traumatic anterior inferior glenohumeral instability were selected. SURGICAL TECHNIQUE: the flexible drill device is inserted into the shoulder joint through the posterior portal and the guide pipe unit is placed 5mm posterior to the margin of the anterior glenoid rim. The flexible drill is driven through the glenoid with the power drill, creating a hole in the glenoid. A non-absorbable suture is passed through the hole and a sliding knot tying is performed over the capsule and labrum after completing stitches with the suture hook loaded. The same procedures are repeated in the 2, 3 and 4 o'clock positions of the glenoid. There was no recurrence of dislocation at the mean follow-up period of 52.3 months. The mean Rowe score was 89.5.

Structural and toxic effect investigation of vanadium pentoxide.

A facile inorganic complex synthesis route has been developed to synthesis V2O5 nanostructures. The effects of varying incubation time on the crystallinity and morphology of the V2O5 phase has been investigated. The obtained XRD result clearly revealed the pure orthorhombic V2O5 crystalline phase. Raman antiphase bridging VO and chaining VO stretching modes peaks at 686 and 521cm(-1) attributed orthorhombic V2O5 characteristics. The V2p3/2 peak at the binding energies of 517eV and V2p1/2 peak at 524eV assigned to V(5+) oxidation state. Bioinspired V2O5 nanostructures as a biocompatible material for anticancer agents show excellent cytotoxicity at higher V2O5 concentration.

Silencing of Twist1 sensitizes NSCLC cells to cisplatin via AMPK-activated mTOR inhibition.

Twist1 is highly expressed in primary and metastatic non-small cell lung cancer (NSCLC), and thus acts as a critical target for lung cancer chemotherapy. In the current study, we investigated the underlying mechanism initiated by silencing of Twist1 that sensitizes NSCLC cells to cisplatin. Silencing of Twist1 triggered ATP depletion, leading to AMP-activated protein kinase (AMPK)-activated mammalian target of rapamycin (mTOR) inhibition in NSCLC cells. AMPK-induced mTOR inhibition, in turn, resulted in downregulation of ribosome protein S6 kinase 1 (S6K1) activity. Downregulation of mTOR/S6K1 reduced Mcl-1 protein expression, consequently promoting sensitization to cisplatin. Overexpression of Mcl-1 reduced PARP cleavage induced by cisplatin and Twist1 siRNA, suggesting that this sensitization is controlled through Mcl-1 expression. Interestingly, cells treated with Twist1 siRNA displayed upregulation of p21(Waf1/CIP1), and suppression of p21(Waf1/CIP1) with specific siRNA further enhanced the cell death response to cisplatin/Twist1 siRNA. In conclusion, silencing of Twist1 sensitizes lung cancer cells to cisplatin via stimulating AMPK-induced mTOR inhibition, leading to a reduction in Mcl-1 protein. To our knowledge, this is the first report to provide a rationale for the implication of cross-linking between Twist1 and mTOR signaling in resistance of NSCLC to anticancer drugs.

TXNIP potentiates Redd1-induced mTOR suppression through stabilization of Redd1.

The mammalian target of rapamycin (mTOR) is a highly conserved serine-threonine kinase activated in response to growth factors and nutrients. Because of frequent dysregulation of the mTOR signaling pathway in diverse human cancers, this kinase is a key therapeutic target. Redd1 is a negative regulator of mTOR, mediating dissociation of 14-3-3 from tuberous sclerosis complex (TSC)2, which allows formation of a TSC-TSC2 complex. In the present study, we identify TXNIP that inhibits mTOR activity by binding to and stabilizing Redd1 protein. Redd1 and TXNIP expression was induced by a synthetic glucose analog, 2-deoxyglucose (2-DG). Moreover, Redd1 expression in response to 2-DG was regulated by activating transcription factor 4 (ATF4). Overexpression of TXNIP was associated with reduced mTOR activity mediated by an increase in Redd1 level, whereas knockdown of TXNIP using small interfering RNA resulted in recovery of mTOR activity via downregulation of Redd1 during treatment with 2-DG. Interestingly, Redd1 was additionally stabilized via interactions with N-terminal-truncated TXNIP, leading to suppression of mTOR activity. Our results collectively demonstrate that TXNIP stabilizes Redd1 protein induced by ATF4 in response to 2-DG, resulting in potentiation of mTOR suppression. To the best of our knowledge, this is the first study to identify TXNIP as a novel member of the mTOR upstream that acts as a negative regulator in response to stress signals.

Prevention of premature senescence requires JNK regulation of Bcl-2 and reactive oxygen species.

Premature senescence is considered as a cellular defense mechanism to prevent tumorigenesis. Although recent evidences show that c-Jun N-terminal kinase (JNK) is involved in the senescence process, the mechanism for this regulation is not fully understood. Here, we examined the role of JNK in premature senescence of tumor cells. Treatment of cells with the JNK-specific inhibitor SP600125 caused phenotypical changes of senescence and triggered a rapid increase in mitochondrial reactive oxygen species (ROS) production and DNA-damage response (DDR) in MCF7 breast carcinoma cells. ROS generation was attributed to the suppression of B-cell lymphoma-2 (Bcl-2) phosphorylation, and resulted in DNA damage and p53 activation. Bax did not change their localization to the mitochondria, which is required for apoptosis. The essential roles of JNK and phosphorylated Bcl-2 in preventing premature senescence were confirmed using RNA interference and ectopic expression of mutants of Bcl-2, including phosphomimetic and nonphosphorylatable forms. These findings were evidenced in H460 lung carcinoma cells and primary human embryonic fibroblasts. Altogether, our results showed that loss of JNK activity triggers a Bcl-2/ROS/DDR signaling cascade that ultimately leads to premature senescence, indicating that basal JNK activity is essential in preventing premature senescence.

Ultrastructural observation of electron irradiation damage of lamellar bone.

The ultrastructure of murine femoral lamellar bone and the effect of electron irradiation (200 kV) on collagen and mineral features were investigated using in situ high resolution transmission electron microscopy (HRTEM). Bands of collagen fibrils were mostly aligned parallel to the long axis of the bones, with some bands of fibrils inclined in longitudinal sections. The similarity of the ultrastructure between the longitudinal and transverse sections supports the rotated plywood structure of the lamellar bone. The collagen fibrils appeared damaged and the mineral crystals were coarsened after electron irradiation. Continuous diffraction rings became spotty and the contrast between rings and the background became sharper, further suggesting coarsening of apatite crystals and increased crystallinity after irradiation. No new phases were observed after irradiation. Both the damage to collagen and coarsening of apatite crystals can deteriorate the strength and integrity of bone, and may provide insight into fracture in patients who have undergone radiation therapy.

Production of penicillic acid by Aspergillus sclerotiorum CGF.

The production of penicillic acid by Aspergillus sclerotiorum CGF for the biocontrol of Phytophthora disease was investigated in submerged fermentation using media composed of different nutrients. Soluble starch was found to be the most effective substrate among the carbon sources used, and produced the highest penicillic acid concentration of 2.98 mg ml(-1). When organic nitrogen sources were used, pharmamedia, yeast extract, and polypeptone-S were found to be suitable organic nitrogen sources (2.46-2.71 mg ml(-1)). The production of penicillic acid was not detected in when inorganic nitrogen sources were used. Only Na2HPO4, among the metal ions and phosphate salts tested, increased the production of penicillic acid (approximately 20%). When A. sclerotiorum CGF was cultured in optimal medium [8.0% (w/v) soluble starch, 0.6% (w/v) yeast extract, and 0.3% (w/v) Na2HPO4], maximum penicillic acid concentration (approximately 9.40 mg ml(-1)) and cell mass (approximately 17.4 g l(-1)) were obtained after 12 days.

Tumor necrosis factor-related apoptosis inducing ligand (TRAIL)-induced apoptosis is dependent on activation of cysteine and serine proteases.

We examined the role of caspases and serine protease(s) in cell death induced by tumour necrosis factor-related apoptosis-inducing ligand (TRAIL). After incubation of adenocarcinoma cells with TRAIL, caspase-3, -8 were activated and the cleavage of Bid induced the release of cytochrome c, from the mitochondria to the cytosol. Tetrapeptide inhibitors of caspase-1, -2, -3, and -8 suppressed DNA fragmentation and attenuated the release of cytochrome c, whereas inhibitors of caspase-5 did not. Interestingly, the general serine protease(s) inhibitor 4-(2-aminoethyl)benzylsulfonyl fluoride (AEBSF) resulted in the arrest of apoptosis. However, the AEBSF did not prevent the release of mitochondrial cytochrome c during TRAIL-induced apoptosis. From these results, we postulate that serine protease(s) may be involved in post-mitochondrial apoptotic events, that lead to the activation of the initiator, caspase-9.

Growth-inhibitory effect of adenovirus-mediated p53 gene transfer on medulloblastoma cell line, Daoy, harboring mutant p53.

To improve the survival rate, gene therapy, such as the replacement of inactivated tumor suppressor genes, has become a new investigational adjuvant treatment modality for human malignancies. We investigated the effect of adenovirus(Ad)-mediated transfer of wildtype p53 tumor suppressor gene on the medulloblastoma cell line, Daoy, which harbors mutant-type p53 gene. At 50 multiplicity of infection (moi), immunohistochemical staining with p53 monoclonal antibody showed positive staining in all cells 2 days after Ad-CMV-p53 infection. The high expression of wild-type p53 protein was detected in Ad-CMV-p53-infected cells, and expression of wild-type p53 protein peaked on day 2 after the infection. The growth of Ad-CMV-p53-infected cells was greatly suppressed in vitro, and the Ad-CMV-p53 treatment significantly reduced the tumor mass in vivo. The mean weight of Ad-CMV- infected tumors was only 16% of those which were mock infected, and 25% of those which were Ad-CMV-beta-gal infected. On microscopic examination, Ad-CMV-p53-infected tumors showed numerous apoptotic bodies. This Ad-CMV-p53 gene transfer showed high transduction efficacy and expression, resulting in significant growth inhibition of Daoy harboring mutant type p53.

Protein kinase C activation by PMA rapidly induces apoptosis through caspase-3/CPP32 and serine protease(s) in a gastric cancer cell line.

Phorbol 12-myristate 13-acetate (PMA) rapidly induced cell death in SNU-16 gastric adenocarcinoma cells. DNA ladder formation and caspase-3/CPP32 activation were observed in PMA treated cells indicating that PMA induces apoptosis. z-DEVD-fmk, specific inhibitor of caspase-3/CPP32, inhibited the induction of apoptosis by PMA, demonstrating that caspase/CPP32 are critically involved in PMA-induced apoptosis. The serine protein inhibitor 4-(2-aminoethyl)benzenesulfonyl fluoride effectively blocked apoptosis, and also prevented caspase-3/CPP32 activation. Go6983, a specific inhibitor of PKC, almost completely suppressed apoptosis and caspase-3/CPP32 activation. Furthermore, 1,2-dihexanoyl-sn-glycerol, an endogenous activator of PKC, induced apoptosis detected by DNA fragmentation and Hoechst 33258 nuclear staining. From these results, we conclude that PMA is not only a tumor promoter, but can also induce apoptosis in gastric cancer cells. PMA-induced apoptosis appears to be mediated through activation of protein kinase C, and the activation of serine protease(s) and caspase-3/CPP32 may be the molecular mechanisms by which PMA induces apoptosis.

Influence of glutathione S-transferase M1 and T1 genotypes on larynx cancer risk among Korean smokers.

Glutathione S-transferase (GST) isoenzymes are involved in the detoxification of major carcinogens present in tobacco smoke. It is thus conceivable that deficiency in GST activity due to homozygous deletions of the GSTM1 and GSTT1 genes (the null genotypes) may modulate susceptibility to smoking-induced cancers. The influence of the GSTM1 and GSTT1 null genotypes on larynx cancer risk among the Korean population were evaluated using peripheral blood DNA from 82 larynx cancer patients and 63 healthy controls, all of whom were male current smokers. Increased larynx cancer risk was related to the GSTM1 null genotype (odds ratio (OR)=3.53, 95% confidence interval (CI)=1.27-9.83). The OR associated with the GSTT1 null genotype was also increased, but did not reach statistical significance (OR=1.83, 95% CI=0.70-4.79). Individuals lacking both the GSTM1 and GSTT1 genes were at a significantly higher risk for larynx cancer than individuals with both genes present (OR=4.04, 95% CI=1.33-12.30). These data confirm that the GSTM1 null genotype is an important risk modifier for larynx cancer among Korean smokers and combined GSTM1 and GSTT1 null genotypes could be a useful predictor of genetic susceptibility to larynx cancer.

Growth inhibitory effect on glioma cells of adenovirus-mediated p16/INK4a gene transfer in vitro and in vivo.

The tumour suppressor gene p16/INK4a encodes a specific inhibitor of the cyclin D-dependent kinases CDK4 and CDK6. p16/INK4a prevents the association of CDK4 with cyclin D1, and subsequently inhibits phosphorylation of retinoblastoma tumour suppressor protein (pRb), thus preventing exit from the G1 phase. In human cancers, the estimated frequency of genetic alteration involving the p16/INK4a locus is believed to be second only to alteration of p53. A high frequency (greater than 50%) of homozygous p16/INK4a gene deletion has been demonstrated in glioblastoma tissues and p16/INK4a is altered in 80% of glioma cell lines. Therefore, restoration of p16/INK4a would suppress cell proliferation and induce cell growth arrest. We showed here that restoration of p16/INK4a expression in p16 negative U87MG, U251MG and partially deleted U373MG by Ad-CMV-p16/INK4a induced growth suppression in vitro and in vivo. Expression of p16 transferred by Ad-CMV-p16/INK4a in glioma cells was highly efficient and maintained for more than seven days. In addition, we found that the endogenous status of p16 and Rb might affect the expression of exogenous p16/INK4a gene and inhibitory effect of cell proliferation. Even though, there were several factors affecting the efficiency of Ad-CMV-p16/INK4 gene transfer, our results suggest that Ad-CMV-p16 gene therapy strategy is potentially useful and warrants further clinical investigation for the treatment of gliomas.

Mitomycin C induces apoptosis in a caspases-dependent and Fas/CD95-independent manner in human gastric adenocarcinoma cells.

We investigated the mechanism of mitomycin C (MMC)-induced apoptosis in SNU-16 human gastric adenocarcinoma cells. Caspase-8 and caspase-3 were activated in MMC-treated cells whereas caspase-1 was not activated, and cytochrome c was released from mitochondrial membrane to cytosol suggesting that caspase-9 was activated during the MMC-induced apoptotic process. Protein kinase C (PKC) delta was cleaved to its characteristic 40 kDa fragment in a caspase-3-dependent manner; on the other hand PKC zeta was cleaved to approximately 40 kDa independently of caspase-3 in the drug-induced apoptosis of the cells. Incubation with z-DEVD-fmk and benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk) almost completely abrogated MMC-induced DNA fragmentation, indicating that activation of these caspases was crucially involved in MMC-induced apoptosis. Activation of caspase-8 in response to Fas triggering by recruitment of caspase-8 to the Fas has also been found, however, MMC did not induce FasL and Fas expression, as evidenced by reverse transcriptase-polymerase chain reaction and Western blotting. Taken together, these findings indicate that MMC-induced apoptosis in SNU-16 cells was mediated by caspase-8, caspase-9, and caspase-3 activation independently of FasL/Fas interactions.

Protein kinase C activation by phorbol ester increases in vitro invasion through regulation of matrix metalloproteinases/tissue inhibitors of metalloproteinases system in D54 human glioblastoma cells.

To elucidate possible mechanisms of phorbol 12-myristate 13-acetate (PMA) induced in vitro invasiveness of glioblastoma cells, we examined expression levels of membrane-type 1 matrix metalloproteinase (MT1-MMP), MMP-2, MMP-9 and tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 using Western blotting and gelatin zymography assay, and found that PMA induced the secretion of MMP-9, activated MMP-2 proenzyme to fully active form of 59 kDa, down-regulated the TIMP-1 and TIMP-2 secretion, and increased MT1-MMP on the cell surface. However, PKC inhibitor Go 6983 reversed all of these effects brought about by PMA. We, therefore, conclude the activation of PKC by PMA in these cells plays a critical role in the regulation of MMPs/TIMPs system, which has a major role in tumor invasion and metastasis.

Matrix metalloproteinases in human gliomas: activation of matrix metalloproteinase-2 (MMP-2) may be correlated with membrane-type-1 matrix metalloproteinase (MT1-MMP) expression.

To evaluate possible roles of matrix metalloproteinase (MMP)-1, -2, tissue inhibitor of metalloproteinase (TIMP)-1, -2 and membrane-type-1 matrix metalloproteinase (MT1-MMP) in invasion of human gliomas, expressions of these proteins were investigated in ten cases of human glioma and two meningioma tissues and eight human glioma cell lines. In gelatin zymography, MMP-2 activities of glioblastomas were higher than astrocytomas. The activated form of MMP-2 was seen in five of six cases of glioblastomas, but not in astrocytomas. MMP-9 activity was detected in all cases of malignant astrocytomas but the reactivity of MMP-9 was weaker than that of MMP-2. MT1-MMP mRNA expression in glioblastomas was higher than that in astrocytomas. Five cases of glioblastomas with activated form of MMP-2 had MT1-MMP expressions. In vitro, human glioma cell lines with high expression of MT1-MMP also showed high MMP-2 activity. TIMP-1 transcripts were constitutively present in almost all glioma tissues and cell lines, whereas TIMP-2 mRNA were weak especially in malignant gliomas. Imbalance of TIMP-2/MMP-2 was observed using immunoprecipitation analysis in a glioma cell line. High expression of MMP-2 and MT1-MMP is possibly involved in invasiveness of malignant glioma.

Clinical usefulness of serum and plasma vascular endothelial growth factor in cancer patients: which is the optimal specimen?

Vascular endothelial growth factor (VEGF) is secreted by various human cancer cells and plays a key role in cancer angiogenesis and metastasis. Recently, evidence of VEGF storage in blood cells including platelets has been reported. The serum VEGF levels were reported to increase during clotting as a result of its release from platelets, and plasma sample instead of serum was recommended for measuring the circulating VEGF more accurately. However, platelets have been implicated in tumor metastasis since circulating tumor cells forming aggregates with platelets were observed. The purpose of this study was to clarify which is an optimal specimen to measure VEGF in cancer patients, serum or plasma. We measured serum and plasma VEGF levels and platelet counts in 173 cancer patients and 42 healthy people, and found that serum VEGF levels were significantly higher than matched plasma VEGF and the VEGF difference (serum VEGF - plasma VEGF) correlated with platelet counts (r=0.624, p<0.05) in both cancer patients and healthy controls. We selected cancer patients with normal platelet counts (130-400x103/microl, Plt-normal cancer group). Interestingly, serum VEGF levels were higher in Plt-normal cancer group than in healthy controls. The theoretical platelet-derived VEGF in serum, calculated based on actual blood platelet counts (pg per 106 platelets), was also significantly higher in Plt-normal cancer group than in normal controls. It is, therefore, suggested that, although the serum VEGF levels are affected by blood platelets, platelet-derived VEGF also reflect biology of cancer cells, and that serum would be the more useful specimen for measurement of circulating VEGF in cancer patients for prognosis.

TNF-alpha induces apoptosis mediated by AEBSF-sensitive serine protease(s) that may involve upstream caspase-3/CPP32 protease activation in a human gastric cancer cell line.

In the present study, we investigated the role of caspase-3/CPP32 and serine protease(s) in cell death induced by TNF-alpha in SNU-16 human gastric adenocarcinoma cells. Apoptosis induced in SNU-16 cells by TNF-alpha was accompanied by the activation of caspase-3/CPP32. After treatment with TNF-alpha, PKCdelta cleaved to its characteristic 40 kDa fragment in a caspase-3/CPP32 dependent manner. Incubation with z-DEVD-fmk completely abrogated TNF-alpha-induced DNA fragmentation, indicating that activation of caspase-3/CPP32 was crucially involved in TNF-alpha-induced apoptosis. In addition, serine protease inhibitor, 4-(2-aminoethyl)benzenesulfonyl fluoride (AEBSF), clearly inhibited all the features of apoptosis including DNA fragmentation and chromatin condensation. Furthermore, in the AEBSF treated SNU-16 cells, only intact PKCdelta was detected by immunoblot analysis, suggesting that activation of caspase-3/CPP32 was blocked. Thus, the AEBSF-sensitive step may involve an upstream caspase-3/CPP32 protease activation. Taken together, these results suggest that both caspase-3/CPP32 and serine protease(s) are activated and play an important role in TNF-alpha induced apoptosis in SNU-16 cells.

Changes in natural killer cell activity and prostaglandin E2 levels during the progression of diethylnitrosamine-induced hepatocarcinogenesis in Fischer 344 rats.

The sequential changes of natural killer cell (NK) activity and prostaglandin E2 (PGE2) during hepatocarcinogenesis induced by diethylnitrosamine (DEN) in male Fischer 344 rats were investigated. DEN at a concentration of 40 ppm was administered in drinking water for 10 weeks. At weeks 5, 10, 20 and 30, rats were autopsied and the development of glutathione S-transferase placental form positive foci (GST-P+ foci) at weeks 5 and 10 and hepatocellular tumors at weeks 20 and 30 were examined. The labeling index of bromodeoxyuridine (BrdU) an indicator of DNA synthesis, was also sequentially checked. GST-P+ foci were found to increase with age. Hepatocellular nodules increased until week 20, but by week 30 when the incidence of hepatocellular carcinoma was 100%, the incidence of nodules had decreased. BrdU positive cells also increased with age, and by week 30 when the incidence of hepatocellular carcinoma was 100%, the number of BrdU-positive cells had decreased. NK cell activity increased until week 10, but at week 20, was less than in the untreated control group. The level of PGE2 increased until week 5, but at week 10, levels were not significantly different from those seen in the untreated control group. On the basis of these results, we concluded that NK activity is closely related to the progression of hepatocarcinogenesis, but PGE2 levels show no significant change.

Antigenic diversity and serotypes of Helicobacter pylori associated with peptic ulcer diseases.

OBJECTIVES: Clinical presentation of Helicobacter pylori (H. pylori) infection has marked variation mainly due to the strain diversity and host susceptibility. Although H. pylori is identified as a major risk factor for gastric and duodenal ulcers, the ulcerogenic or pathogenic strain has not been documented yet. The objective of this study was to investigate antigenic types of the ulcerogenic strain of H. pylori. METHODS: The sera of 64 patients were tested by Western blot using Helicoblot 2.0 for six major anti-H. pylori antibodies, together with CLO test and histological examination of gastric biopsy tissues. Thirty-five, nine and 20 patients had duodenal ulcer, gastric ulcer and chronic active gastritis, respectively. The antigenic types of H. pylori were analyzed in 54 patients with positive H. pylori infection. In this study, H. pylori was divided into four serotypes according to the presence and absence of CagA and VagA: type I; CagA (+) and VacA(+), type Ia: CagA (+) and VacA(-), type Ib: CagA(-) and VacA(+), and type II: CagA(-) and VacA(-). RESULTS: There was no difference in the number of bands for six antigens: 3.2 +/- 1.4, 3.0 +/- 1.2 and 3.1 +/- 1.4 in 35 duodenal ulcer, 7 gastric ulcer and 12 chronic gastritis, respectively. The band with 119 kDa was 90.7%, which was the most common band with the order of 35, 30, 26.5, 89 and 19.5 kDa. Type I, la and Ib were positive in 22.2, 42.6 and 27.8%, respectively, which were significantly higher than type II (p < 0.05). There was no difference in the positive rates of four urease subtypes between the four serotypes.